The action of beta-bungarotoxin on neuromuscular junctions will be studied by a combination of electrophysiological, biochemical and anatomical techniques. We know from our earlier studies that the toxin is acting as a phospholipase when it destroys synaptic transmission. Our current problem is to decide if the selective hydrolysis of nerve terminal phospholipids is due to substrate specificity, inability of the nerve terminal to re-synthesize phospholipids or due to a recognition site on the nerve terminal quite distinct from the substrate. We are exploring some of these questions in the marine ray Narcine brasiliensis. BIBLIOGRAPHIC REFERENCES: Oberg, S.G. & Kelly, R.B. (1976). The mechanism of beta-bungarotoxin action. I. Modification of transmitter release at the neuromuscular junction. J. Neurobiol. 7:129-141. Strong, P., Goerke, J., Oberg, S. & Kelly, R.B. (1976). Beta-bungarotoxin, a presynaptic toxin with enzymatic activity. Proc. Nat. Acad. Sci. USA 73: 178-181.